CXCL3 was reportedly associated with the invasion and metastasis of various malignancies, the role of CXCL3, however, in preeclampsia has not been fully discussed. We previously found placental CXCL3 level in severe preeclampsia was significantly lower than that in healthy pregnancy and exogenous recombinant human CXCL3 protein was able to promote trophoblasts' migration and proliferation. The current study, therefore, is further to investigate effects of endogenous CXCL3 on migration, invasion, proliferation, tube formation and apoptosis of trophoblasts. Immunofluorescence staining demonstrated that CXCL3 localized in both trophoblasts of placenta and HTR-8/SVneo cells. Moreover, data showed that migration, invasion, proliferation and tube-formation capability of HTR-8/SVneo cells transfected with siRNA-CXCL3 were suppressed by down-regulation of CXCL3, while those behaviors of HTR-8/SVneo cells transfected with pEZ-CXCL3 were enhanced by upregulation of CXCL3. Nevertheless, the apoptosis of HTR-8/SVneo cells was not affected by neither siRNA nor overexpression plasmid. The result suggests that CXCL3 is involved in migration, invasion, proliferation and tubule formation of trophoblasts and may play a key role in the pathogenesis of preeclampsia.
Keywords: CXCL3; Chemokine; Pathogenesis; Preeclampsia; Trophoblast.
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